Isaac Newton’s groundbreaking scientific productivity while isolated from the spread of bubonic plague is legendary. University of California San Diego physicists can now claim a stake in the annals of pandemic-driven science.
A team of UC San Diego researchers and colleagues at Purdue University have now simulated the foundation of new types of artificial intelligence computing devices that mimic brain functions, an achievement that resulted from the COVID-19 pandemic lockdown. By combining new supercomputing materials with specialized oxides, the researchers successfully demonstrated the backbone of networks of circuits and devices that mirror the connectivity of neurons and synapses in biologically based neural networks.
The simulations are described in the Proceedings of the National Academy of Sciences (PNAS).
Wageningen is one of a clutch of research institutions globally that hold patents on CRISPR, a technique that enables precise changes to be made to genomes, at specific locations. Other institutions — including the Broad Institute in Cambridge, Massachusetts, and the University of California, Berkeley, which have some of the largest portfolios of patents on the subject — also provide CRISPR tools and some intellectual property (IP) for free for non-profit use. But universities could do better to facilitate access to CRISPR technologies for research.
Universities hold the majority of CRISPR patents. They are in a strong position to ensure that the technology is widely shared for education and research.
A cancer treatment that uses messenger RNA to launch an immune attack on cancer cells can completely shrink tumours in mice and is now being tested in people.
Messenger RNAs – or mRNAs – are molecules that instruct cells to make proteins. They have risen to fame with the roll out of mRNA covid-19 vaccines.
Exploring The Gut Microbiota-Brain Axis In Health, Disease, and Aging — Dr. Marina Ezcurra, Ph.D. University of Kent.
Dr. Marina Ezcurra (https://marinaezcurralab.com/) is a Lecturer in the Biology of Aging, and NeuroBiology, at the School of BioSciences, at the University of Kent, UK (https://www.kent.ac.uk/biosciences/people/2081/ezcurra-marina).
Dr. Ezcurra received her PhD from the Karolinska Institute in 2011. Her PhD research was a collaborative project between Karolinska and the Medical Research Council Laboratory of Molecular Biology at Cambridge, where she studied neural circuits and behavior using C. elegans in the lab of Dr. Bill Schafer.
During her PhD, Dr. Ezcurra identified extra-synaptic mechanisms by which nutritional status modulates nociception, involving neuro-peptidergic and dopaminergic signaling. She went on to do a postdoc working on aging with Dr. David Gems at University College London.
During her postdoc, Dr. Ezcurra developed methods to monitor the development of multiple age-related diseases in-vivo in C. elegans, leading to the discovery of a previously unknown process, Intestinal Biomass Conversion. This mechanism enables the C. elegans intestine to be broken down to produce vast amounts of yolk, resulting in poly-morbidity and mortality in aging nematodes. This work illustrates how aging and age-related diseases can be the result of run-on of wild-type gene function, rather than stochastic molecular damage.
Current research in Dr. Ezcurra’s group focuses on how host-microbiome interactions affect host aging, and is funded by The Wellcome Trust and Royal Society.
Dr. Ezcurra is a trustee board member of The British Society of Research on Aging.
People with rare disorders that cause shortened telomeres—protective caps that sit at the end of chromosomes—may be more likely to have blood cancers such as leukemia or myelodyplastic syndrome. Now, Johns Hopkins Medicine scientists have discovered several “self-correcting” genetic mutations in bone marrow that may protect such patients from these cancers.
In a study published online August 3 2021, in the Journal of Clinical Investigation, the researchers also suggest these mutations can serve as biomarkers that may indicate if patients with short telomere syndromes are likely to develop blood cancers.
“These are the most common cancers we see in patients with short telomere syndromes,” says Mary Armanios, M.D., director of the Telomere Center and professor of oncology at the Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins. “We know that at a certain point, the cells of patients with shortened telomeres either become cancerous or stay healthy.”
Summary: Researchers have identified 2,000 genes in humans linked to longevity. The genes are associated with biological mechanisms that drive the prolongation of life in mammals, including DNA repair, coagulation, and immune response.
Source: UPF Barcelona.
What determines the life expectancy of each species? This is a fundamental and highly complex question that has intrigued the field of research throughout history. From the evolutionary point of view, the major cause of these differences between species lies in their ecological adaptations. For example, life expectancy is longer in species adapted to living in trees, underground, or with large body mass, since all these adaptations reduce mortality by predation.
I recently set sail on Sunwater Marine’s Ramblin’ Rose, a 40-foot sailing yacht powered by solar panels and electric propulsion.
While we at Electrek often tend to focus on electric vehicles taking over roads, it’s important to remember that our inevitable abandonment of fossil fuels stems to all modes of transportation, whether it’s by land, air, or even the sea. I recently had the opportunity to set sail on Sunwater Marine’s Ramblin’ Rose, a 40-foot sailing yacht powered by solar panels and electric propulsion. It’s one of the only vessels of its kind on the West Coast.
It was founded by president James Richmond in 2,020 amid the global pandemic. Richmond had a little more free time to search for a boat for blue water cruising to which he could add solar.
A new interpretation of quantum mechanics sees agents as playing an active role in the creation of reality. Blake Stacey outlines the case for QBism and its radical potential.
The pandemic shut down our university when I was in the middle of giving a lecture. We had been anticipating the possibility for a few days, but it was still impeccable timing. I finished my spiel, out came the phones, and suddenly we weren’t going to see each other post-spring break after all. For the rest of the term, I did what so many teachers found themselves doing: gamely trying to soldier on. I scrounged and borrowed a whiteboard, easel and webcam, set myself up in the nicest light the house had to offer, and did my best to convey graduate-level physics to an audience of tiny rectangles. And like so many other teachers, I learned there’s nothing like a radical change of circumstances for driving one to re-evaluate what the essential ideas of a subject must be.
Common medications can accumulate in gut bacteria, a new study has found, altering bacterial function and potentially reducing the effectiveness of the drug. These interactions—seen for a variety of medications, such as depression, diabetes, and asthma drugs—could help researchers to better understand individual differences in drug effectiveness and side-effects, according to the study published in Nature.
It is known that bacteria can chemically modify some drugs, a process known as biotransformation. This study, led by researchers from the Medical Research Council (MRC) Toxicology Unit at the University of Cambridge and the European Molecular Biology Laboratory (EMBL) in Germany, is the first to show that certain species of gut bacteria accumulate human drugs, altering the types of bacteria and their activity.
This could change the effectiveness of the drug both directly, as the accumulation could reduce the availability of the drug to the body, and indirectly, as altered bacterial function and composition could be linked to side-effects.
